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Management of Temporomandibular Disorders II

Several of the common temporomandibular joint (TMJ) disorders encountered during dental treatment are 1) temporomandibular joint sounds, 2) change in jaw range of motion, 3) referred pain to the temporomandibular joints, masticatory muscles, teeth, and ears, and 4) changes in the occlusion. Whereas Part I of this presentation addressed TMJ sounds, the presentation that follows herein will highlight changes in motion, pain, and changes to the patient’s occlusion.


Change in Jaw Range Motion

A change in jaw range of motion can be due to joint-related disorders or muscle-related disorders. The change may manifest as an acute, intermittent, or chronic closed lock (anterior dislocation of the TMJ disc) or an open lock of the jaw (hypermobility, subluxation or dislocation of the TMJ). A decrease in jaw range of motion caused by muscle-related disorders is usually caused by myofascial pain and is commonly known as trismus. Management of myofascial pains is discussed under referred pains.


Anterior Dislocation of the TMJ Disc (Closed Lock)

In this disorder, the posterior band of the TMJ disc moves from the top of the mandibular condyle (12-o’clock position) to a more downward and forward position on the posterior slope of the articular eminence (eg, 3-o’clock position). Prior to the disc dislocation, the mandible is able to negotiate its way beneath the posterior band to the intermediate band, causing a popping sound. Following disc dislocation, the condyle can no longer negotiate its way to its usual position beneath the articular disc due to the mechanical blockage caused by the posterior band of the articular disc. This often causes a significant restriction in jaw sagittal movements to approximately 25 mm of interincisal distance (Figure 1).

The diagnosis of disc dislocation is best established by MRI of the joint.1 Symptoms of dislocation of the TMJ disc include restriction of sagittal jaw opening to within 25 mm with significant deflection to the affected side, restricted lateral mandibular movement to the opposite side but not to the affected side, and history of TMJ clicking sounds but absence of these sounds when the disc is dislocated. These symptoms can be easily explained by the inability of the mandibular condyle to translate forward because of the presence of a mechanical obstacle (posterior band of the articular disc) anterior to the condyle.

If attempted within a few hours, reduction (treatment) of the acutely dislocated TMJ disc consists of pressing downward on the most posterior mandibular molar of the affected side. While the clinician is pressing downward, the patient attempts to translate the mandibular condyle quickly and repeatedly, to the opposite side. If the reduction is successful, a pop may be heard, and the patient will be able to open the mouth as wide as prior to the dislocation. This movement is usually followed by pain reducing measures, such as nonsteroidal antiinflammatory drugs, moist heat, and possibly a stabilization splint or an anterior positioning splint. If the attempts at reducing disc dislocation are unsuccessful, local anesthesia of the joint, nitrous oxide sedation, moist heat, and ultrasound application may be utilized. These techniques relax the patient and the muscles, thereby aiding reduction of the dislocation.

If disc dislocation becomes recurrent despite the above measures, wearing an anterior positioning splint during sleep or for several hours each day may become necessary. Anterior positioning splints (Figures 2 and 3) maintain the mandible in the least protruded position, at which there is no clicking noise or locking sensation, and the jaw movement is smooth and uninterrupted. If the above measures do not succeed in alleviating the locking, the anterior positioning splint may have to be worn for 24 hours per day. Under these circumstances, permanent changes in the patient's occlusion may result, due to the protruded jaw position. These changes are usually unilateral or bilateral posterior open bite; sometimes an anterior open bite may result. These conditions necessitate orthodontic treatment or, on rare occasions, orthognathic surgery. When anterior positioning splint therapy is attempted, the potential consequences of changes in the occlusion must be explained to the patient.

If treatment is not sought following the occurrence of anterior dislocation of the TMJ disc, due to the absence of significant pain, metaplasia of the retrodiscal tissues2 into a new fibrous pseudodisc may occur. It is also possible that normal range of jaw motion will return (Figure 4). This natural process of healing occurs frequently as evidenced by the disc dislocation studies in cadavers10 and asymptomatic volunteers. If the natural healing process does not occur, and the retrodiscal tissues as well as the articular disc continue to degenerate, osteoarthritis may occur.


Subluxation (Hypermobility) of the TMJ (Open Lock)

In this condition, the mandible is locked in the wide open position (Figure 5). It may occur while yawning, attempting to take a big bite, or following a lengthy dental appointment. The condyle is maximally protruded on the anterior aspect of the articular eminence, and the mouth is wide open. The patient cannot close the mouth since the mandibular condyle cannot negotiate its way back, posteriorly, past the apex of the articular eminence. Open lock usually occurs bilaterally and may be a result of systemic joint laxity.

Reduction (treatment) of the open lock consists of attempting to distract the mandibular condyles downward past the apices of the articular eminences, one side at a time. The thumbs are wrapped with gauze, and pressure is applied on the last mandibular molar, alternately on each side, until the condyle moves past the articular eminence. At this time, the patient will be able to close his or her mouth, which may occur with a snapping forceful motion, hence the need for the protection of the thumbs.


Myofascial Pain

One of the results of myofascial pains is muscle shortening.3 If the elevator muscles are involved, the patient is not able to open the mouth widely without significant pain―a disorder known as trismus. The etiology of myofascial pains is unknown; the most common source may include overloading during bruxism, lengthy dental appointments, emotional stress, and repeated inferior alveolar nerve local anesthetic injections.

What distinguishes trismus from anterior dislocation (closed lock) of the TMJ disc (in addition to the absence of a history of popping noises) is the character of the end feel of the opening.4 Maximal jaw opening, when measured during disc dislocation (closed lock), is usually a definite site. If the patient is asked to open wider, mouth opening will not increase by more than a few millimeters―a so called “hard end feel.” For example, if a patient’s comfortable opening is 20 mm, maximal opening will be 21 mm or 22 mm. Measuring maximal opening during trismus is not as definite. If the patient is asked to open wider, mouth opening will increase significantly, to a “soft end feel” ―the patient can open comfortably to 34 mm, maximally to 47 mm (Figures 6 and 7). However, this is accompanied by significant pain. During trismus, mouth opening is limited by pain or the fear of pain; during disc dislocation, mouth opening is limited by a mechanical obstacle anterior to the mandibular condyle.

Other than elimination of the etiologic factor, treatment for trismus consists primarily of a carefully detailed systematic palpation of the masticatory and cervical muscles, attempting to identify the muscles that have trigger points or respond with significant pain when palpated. When involved with myofascial pains, accessible muscles (masseter, temporalis, sternomastoid, or trapezius) are treated with the spray-and-stretch technique.3 The muscle is stretched or placed under some tension but not enough to induce pain. The entire length of the skin overlying the muscle is sprayed from origin to insertion in parallel gentle sweeps, in one direction only, with a vapocoolant. The bottle is held approximately 12 inches from the skin, and the coolant is directed at an acute angle of approximately 30o, not perpendicularly. During and immediately following the application, an attempt is made to stretch the muscle to its full length, without inducing pain. The stretching exercise is the most important part of the treatment. Moist heat is then applied to the muscle, while the patient performs a series of gentle exercises attempting to further stretch the muscle. Moist heat is obtained by a heating pad or by wetting a wash cloth, squeezing off the excess water, then placing it in a microwave oven for 1 to 2 minutes. The entire process is repeated three times.

Inaccessible muscles, such as the lateral pterygoid or the temporalis tendon, are best treated by injecting the most painful area with a local anesthetic (patient consent is required). Pain elicited preauricularly when the patient protrudes the mandible (Figure 8) and opens it against resistance (Figure 9) should be diagnosed as myofascial pain in the inferior lateral pterygoid muscle. If these tests are positive in eliciting deep pain preauricularly, the area behind the tuberosity is palpated in a distal and medial direction using the tip of the index finger (Figure 10) or the end of a cotton applicator. If significant pain results, this confirms the diagnosis of myofascial pain of the inferior lateral pterygoid muscle, and the area is injected with local anesthetic.

Temporal tendonitis is suspected if the patient complains of pain between the maxillary and mandibular third molars on the same side, in the absence of local etiologic factors. To confirm the diagnosis, the anterior border of the ascending ramus of the mandible (Figure 11) as well as the coronoid process (Figure 12) are palpated by the tip of the index finger. If significant pain is elicited, local anesthetic solution is injected in the most painful area, followed by stretching the temporalis muscle (opening and closing slowly for approximately 10 times).

A topical anesthetic and aspiration to prevent intravascular injections are recommended prior to intraoral injections. A long 25-gauge needle and 1.8 mL of anesthetic is used for the inferior lateral pterygoid muscle injection. A 27-gauge needle and 1.8 mL or 3.6 mL of anesthetic solution are usually used for the temporalis tendon injections.

Travell and Simons recommend the use of 0.5% procaine without a vasoconstrictor for intramuscular injections.3 In the absence of procaine, Travell and Simons prefer 2% lidocaine over 3% mepivacaine. Long- acting anesthetics, such as bupivacaine, are not recommended. No vasoconstrictor should be used for intramuscular injections for the treatment of myofascial pains due to the possibility of inducing localized muscle necrosis. Following the injection of the local anesthetic, the muscle should be sprayed and stretched, if accessible (eg, temporalis). Moist heat is applied as well. Due to the difficulty in accessing the lateral pterygoid muscle and the temporalis tendon by the patient and the physical therapist, the dentist is best qualified to alleviate these pains.


Referred Patients

The patient may often complain of pain in the teeth, TMJs, or ears, but the source of pain is elsewhere. The teeth should be examined clinically, radiographically, by percussion, and by transmitted light. In absence of other sources, including pulp or tooth fracture, referred pain should be suspected. Usually, referred pain involving the head and neck (with the exception of the sternomastoid) originates from trigger points that are found on the same side as the pain. Using a table compiled from information gained from Travell and Simons’ book,3 the clinician can devise a plan for diagnosis and treatment. If a patient complains of toothache in the maxillary second premolar, in the absence of occlusal, pulpal, periapical, periodontal, tooth fracture, or maxillary sinusitis etiologic factors, a high degree of suspicion should be directed to the left temporal muscle and the left superficial masseter muscle. These muscles should be carefully palpated for the presence of trigger or tender points. If found, the muscle is sprayed with a coolant and stretched. If the diagnosis is correct, the pain should disappear. An infiltration of local anesthetic may be used for differential diagnosis; if bruxism is suspected, a stabilization occlusal splint may be used.


Acute Malocclusion

When a patient with a history of normal occlusion and no recent dental interventions awakens one morning with the ”bite off,” the reason may be temporary changes in the TMJ, such as adhesions or edema, or temporary changes in the muscles with muscle shortening. A detailed examination should be conducted and the source managed as discussed in this article. Usually, the patient is requested to change to a softer diet, to take nonsteroidal antiinflammatory drugs or acetaminophen, as required, and apply moist heat. A soft splint may be used to support the occlusion. In most instances, the acute malocclusion will abate in a few days.



In an average dental practice, the clinician may encounter signs and symptoms related to the TMJ, the masticatory muscles, or the occlusion. The suggestions in this article—as well as Part I that may be beneficial if reviewed in sequence—will enable the clinician to arrive at a diagnosis, counsel the patient, and administer the treatment, if necessary.

*Private Practice, New Orleans, Louisiana



  1. Dolwick MF. Temporomandibular joint disc displacement: Clinical perspectives. In: Sessle BJ, Bryant PS, Dionne RA, eds. Temporomandibular Disorders and Related Pain Conditions. Seattle, WA: IASP Press; 1995:79-85.
  2. Scapino RP. Histopathology associated with malposition of the human temporomandibular joint disc. Oral Surg Oral Med Oral Path 1983;55(4):382-397.
  3. Travell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual. Baltimore, MD: Williams & Wilkins; 1983:219-272.
  4. Hesse JR, Naeije M, Hansson TL. Craniomandibular stiffness toward maximum mouth opening in healthy subjects: A clinical and experimental investigation. J Craniomandib Disord 1990;4(4):257-266.
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